About Me

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Sunday, November 18, 2012

Awilda Jimenez got a scan for Alzheimer’s after she started forgetting
things. It was positive.

By GINA KOLATA Published: November 15, 2012

When Awilda Jimenez started forgetting things last year, her husband,
Edwin, felt a shiver of dread. Her mother had developed Alzheimer’s in her 50s.
Could his wife, 61, have it, too?

He learned there was a new brain scan to diagnose the disease and nervously
agreed to get her one, secretly hoping it would lay his fears to rest. In June,
his wife became what her doctor says is the first private patient in Arizona to
have the test.

“The scan was floridly positive,” said her doctor, Adam S. Fleisher,
director of brain imaging at the Banner Alzheimer’s Institute in Phoenix.

The Jimenezes have struggled ever since to deal with this devastating news.
They are confronting a problem of the new era of Alzheimer’s research: The
ability to detect the disease has leapt far ahead of treatments. There are none
that can stop or even significantly slow the inexorable progression to dementia
and death.

Families like the Jimenezes, with no good options, can only ask: Should
they live their lives differently, get their affairs in order, join a clinical
trial of an experimental drug?

“I was hoping the scan would be negative,” Mr. Jimenez said. “When I found
out it was positive, my heart sank.”

The new brain scan technology, which went on the market in June, is
spreading fast. There are already more than 300 hospitals and imaging centers,
located in most major metropolitan areas, that are ready to perform the scans,
according to Eli Lilly, which sells the tracer used to mark plaque for the scan.

The scans show plaques in the brain — barnaclelike clumps of protein, beta
amyloid — that, together with dementia, are the defining feature of Alzheimer’s
disease. Those who have dementia but do not have excessive plaques do not have
Alzheimer’s. It is no longer necessary to wait until the person dies and has an
autopsy to learn if the brain was studded with plaques.

Many insurers, including Medicare, will not yet pay for the new scans,
which cost several thousand dollars. And getting one comes with serious risks.
While federal law prevents insurers and employers from discriminating based on
genetic tests, it does not apply to scans. People with brain plaques can be
denied long-term care insurance.

The Food and Drug Administration, worried about interpretations of the
scans, has required something new: Doctors must take a test showing they can
read them accurately before they begin doing them. So far, 700 doctors have
qualified, according to Eli Lilly. Other kinds of diagnostic scans have no such
requirement.

In another unusual feature, the F.D.A. requires that radiologists not be
told anything about the patient. They are generally trained to incorporate
clinical information into their interpretation of other types of scans, said Dr.
R. Dwaine Rieves, director of the drug agency’s Division of Medical Imaging
Products.

But in this case, clinical information may lead radiologists to
inadvertently shade their reports to coincide with what doctors suspect is the
underlying disease. With Alzheimer’s, Dr. Rieves said, “clinical impressions
have been misleading.”

“This is a big change in the world of image interpretation,” he said.

Like some other Alzheimer’s experts, Dr. Fleisher used the amyloid scan for
several years as part of a research study that led to its F.D.A. approval.
Subjects were not told what the scans showed. Now, with the scan on the market,
the rules have changed.

Dr. Fleisher’s first patient was Mrs. Jimenez. Her husband, the family
breadwinner, had lost his job as a computer consultant when the couple moved
from New York to Arizona to take care of Mrs. Jimenez’s mother. Paying several
thousand dollars for a scan was out of the question. But Dr. Fleisher found a
radiologist, Dr. Mantej Singh Sra of Sun Radiology, who was so eager to get into
the business that he agreed to do Mrs. Jimenez’s scan free. His plan was to be
the first in Arizona to do a scan, and advertise it.

After Dr. Sra did the scan, the Jimenezes returned to Dr. Fleisher to learn
the result.

Dr. Fleisher, sad to see so much plaque in Mrs. Jimenez’s brain, referred
her to a psychiatrist to help with anxiety and suggested she enter clinical
trials of experimental drugs.

But Mr. Jimenez did not like that idea. He worried about unexpected side
effects.

“Tempting as it is, where do you draw the line?” he asks. “At what point
do you take a risk with a loved one?”

At Mount Sinai Medical Center in New York, Dr. Samuel E. Gandy found that
his patients — mostly affluent — were unfazed by the medical center’s $3,750
price for the scan. He has been ordering at least one a week for people with
symptoms ambiguous enough to suggest the possibility of brain plaques.

Most of his patients want their names kept confidential, fearing an
inability to get long-term care insurance, or just wanting privacy.

A woman from New Zealand was told by one doctor that she had Alzheimer’s
and by another that she had frontotemporal dementia, a rare brain disease that
strikes people at younger ages than Alzheimer’s and progresses faster. She had a
scan. The result was clear — no significant accumulation of plaques. She had
frontotemporal dementia. Unfortunately, Dr. Gandy said, there was nothing he
could offer her, not even a clinical drug trial.

A man given a diagnosis of Parkinson’s disease was totally immobile and
demented. Could he have had Alzheimer’s all along?

A scan showed he did.

Dr. Gandy’s first patient, Alexander Dreyfoos, an 80-year-old electronics
engineer and businessman, was one of the very few willing to be open about his
experience. He is independently wealthy and was not worried about privacy or
insurance.

But he was very worried about Alzheimer’s. His mother, who died at age 79,
had it. “I watched her deteriorate to the point where she couldn’t even
recognize me,” Mr. Dreyfoos said. And he had begun seeing signs that his memory
was slipping.

“A few years ago, I realized I wasn’t at the top of my game,” he said.

Mr. Dreyfoos had his DNA sequenced by a commercial company and learned that
he had a gene, ApoE4, that increases the risk of Alzheimer’s. At Massachusetts
General Hospital, he learned he had shrinkage of his brain — typical of
Alzheimer’s. After doctors tested his memory and reasoning, he said, they told
him he was right to worry.

Finally, Mr. Dreyfoos went to Dr. Gandy at Mount Sinai, looking for an
experimental treatment for the Alzheimer’s he was sure he had. Dr. Gandy also
suspected he had the disease, but suggested a scan.

The scan did not show an abnormal accumulation of amyloid. As far as Dr.
Gandy is concerned, Mr. Dreyfoos does not have Alzheimer’s.

Mr. Dreyfoos was surprised, “wonderfully so,” he said.

Dr. Gandy said that as many as 30 percent of people who seem to have
Alzheimer’s turn out not to have it when they get the scan. But those who get
bad news struggle to cope.

Desperate to slow the progression of his wife’s disease, Mr. Jimenez is now
giving her turmeric, coenzyme Q10, astaxanthin, krill oil, ginkgo biloba and
coconut oil — remedies he found on the Internet. There is no good evidence they
work, and each costs about $5 to $15 a month. But, Mr. Jimenez says: “What am I
going to do? People feel so helpless with this disease that they are willing to
try anything.”

He worries about the future and how they will survive financially. He
wonders if it might have been better not to know the diagnosis.

Results from recent experiments with rodents imply that Alzheimer disease
might be inducible by seeding Aβ peptides into recipient animals. In respect to
this new experimental data, public health aspects as well as epidemiological
data have to be reevaluated. In this article, the available experimental and
epidemiological data are reviewed.

snip...

In summary, epidemiological evidence is extremely difficult to assess in
this context. This is especially true, since case definitions and case detection
rates have changed over time. Given the fact that a potential way of
transmission is not only unknown but that no way of transmission can be excluded
yet, careful assessment is imperative.

Public health implications

In the epidemic of non-communicable diseases AD plays an important role for
morbidity and mortality as well as the associated costs. To date, AD is the 6th
leading cause of death in the US and the projected costs in the US by 2050 are
$1.1 trillion.66

Knowledge about transmissibility is essential in all kinds of epidemics for
prevention, diagnosis and treatment. If AD featured transmission patterns
comparable with those of prion diseases, iatrogenic induction/transmission would
play a major role for public health. Prevention would be first priority and
might include measures such as extended sterilization methods for surgical
instruments as well as identification of patients potentially posing a risk as
well as patients at risk. From a public health perspective also alternate ways
of transmission not evaluated yet must be considered. For prevention to work,
biomarkers for early disease detection must be validated, independently of the
ways of possible induction since the disease itself starts well before clinical
onset. As Sigurdsson stated correctly almost 10 years ago, future research on
therapies might also be limited as long as there is no convincing evidence
against transmissibility of AD.8 This is especially true for vaccination studies
and clinical trials using parts of β-amyloid.

Conclusion

In conclusion, with this short review, we want to encourage a broader
discussion and modern epidemiological research in this context. Well-designed
epidemiologic studies have to be initiated. Methodologically these studies must
be constructed to address the epidemiologically challenging aspects of Alzheimer
disease such as dissociation between first neuropathological alterations and
clinical onset, uncertainties in early diagnosis as well as AD heterogeneity.

This work was supported by a Bundesministerium für Bildung und Forschung
grant within the German Network for Degenerative Dementia (KNDD-2, 2012-2015,
determinants for disease progression in AD, grant no. 01GI1010C), as well as
JPND, EU-FP7 PRIORITY.Authors’ contributions: C.S. was responsible for the
initiation of the project, general conception and the composition of the final
manuscript. A.K. provided parts of the section on epidemiology. C.K. provided
parts of the section on experimental clues regarding AD
transmissibility/inducibility. I.Z. was responsible for the initiation of the
project, the critical review for contentual errors and writing parts of the
conclusion. All authors contributed to the revision of the manuscript. The
authors declare no conflicts of interest.

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both disease, and it’s variants, in many cases are merely
names of the people that first discovered them. Both diseases are incurable and
debilitating brain disease, that are in the end, 100% fatal, with the
incubation/clinical period of the Alzheimer’s disease being longer than the TSE
prion disease. Symptoms are very similar, and pathology is very similar. I
propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation
disease, and that Alzheimer’s is Transmissible, and is a threat to the public
via the many Iatrogenic routes and sources. It was said long ago that the only
thing that disputes this, is Alzheimer’s disease transmissibility, or the lack
of. today, there is enough documented science (some confidential), that shows
that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and
or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and
one that needs to be addressed immediately.

Methods

Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.

Results

The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you
can take the ash and mix it with saline and inject that ash into a mouse, and
the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production as well. the TSE prion agent also survives
Simulated Wastewater Treatment Processes. IN fact, you should also know that the
TSE Prion agent will survive in the environment for years, if not decades. you
can bury it and it will not go away. TSE prion agent is capable of infected your
water table i.e. Detection of protease-resistant cervid prion protein in water
from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it
out and be done with. that’s what’s so worrisome about Iatrogenic mode of
transmission, a simple autoclave will not kill this TSE prion agent.

Conclusions

There should be a Global Congressional Science round table event (one of
scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics let science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already. what’s the use of science progressing human life to
the century mark, if your brain does not work?

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both diseases are incurable and debilitating brain disease,
that are in the end, 100% fatal, with the incubation/clinical period of the
Alzheimer’s disease being longer (most of the time) than the TSE prion disease.
Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long
incubation disease, and that Alzheimer’s is Transmissible, and is a threat to
the public via the many Iatrogenic routes and sources. It was said long ago that
the only thing that disputes this, is Alzheimer’s disease transmissibility, or
the lack of. The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease.

Conclusions

There should be a Global Congressional Science round table event set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics lets science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already.

Ample justification exists on clinical, pathologic, and biologic grounds
for considering a similar pathogenesis for AD and the spongiform virus
encephalopathies. However, the crux of the comparison rests squarely on results
of attempts to transmit AD to experimental animals, and these results have not
as yet validated a common etiology. Investigations of the biologic similarities
between AD and the spongiform virus encephalopathies proceed in several
laboratories, and our own observation of inoculated animals will be continued in
the hope that incubation periods for AD may be even longer than those of CJD.

Our results suggest that some of the typical brain abnormalities associated
with AD can be induced by a prion-like mechanism of disease transmission through
propagation of protein misfolding. These findings may have broad implications
for understanding the molecular mechanisms responsible for the initiation of AD,
and may contribute to the development of new strategies for disease prevention
and intervention. Keywords: amyloid; prion; protein misfolding; disease
transmission

# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy
prion disease, Iatrogenic, what if ? and the opportunity to present it, at the
Alzheimer’s Association International Conference 2012 (AAIC), as a poster
presentation. However, with great sadness, I must regretfully decline the
invitation due to a medical reasons, and traveling to Canada, of which is not
possible. ...

An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.

Methods:

12 years independent research of available data

Results:

I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.

Conclusion:

I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.

From the Division of Viral and Rickettsial Diseases (Drs. Belay and
Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers
for Disease Control and Prevention, Atlanta, GA; and National Prion Disease
Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology,
Institute of Pathology, Case Western Reserve University, Cleveland, OH.

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?

To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...

>>> Up until about 6 years ago, the pt worked at Tyson foods where
she worked on the assembly line, slaughtering cattle and preparing them for
packaging. She was exposed to brain and spinal cord matter when she would
euthanize the cattle. <<<

Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010
in Mesquite Texas.

She left 6 Kids and a Husband.The Purpose of this web is to give
information in Spanish to the Hispanic community, and to all the community who
want's information about this terrible disease.- Physician Discharge Summary,
Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010
Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General
Neurology Team Linda was a Hispanic female with no past medical history presents
with 14 months of incresing/progressive altered mental status, generalized
weakness, inability to walk, loss of appetite, inability to speak, tremor and
bowel/blader incontinence. She was, in her usual state of health up until
February, 2009, when her husbans notes that she began forgetting things like
names and short term memories. He also noticed mild/vague personality changes
such as increased aggression. In March, she was involved in a hit and run
MVA,although she was not injured. The police tracked her down and ticketed her.
At that time, her son deployed to Iraq with the Army and her husband assumed her
mentation changes were due to stress over these two events. Also in March, she
began to have weakness in her legs, making it difficult to walk. Over the next
few months, her mentation and personality changes worsened, getting to a point
where she could no longer recognized her children. She was eating less and less.
She was losing more weight. In the last 2-3 months, she reached the point where
she could not walk without an assist, then 1 month ago, she stopped talking,
only making grunting/aggressive sounds when anyone came near her. She also
became both bowel and bladder incontinent, having to wear diapers. Her
'"tremor'" and body jerks worsened and her hands assumed a sort of permanent
grip position, leading her family to put tennis balls in her hands to protect
her fingers. The husband says that they have lived in Nebraska for the past 21
years. They had seen a doctor there during the summer time who prescribed her
Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the
medications did not help and she continued to deteriorate clinically. Up until
about 6 years ago, the pt worked at Tyson foods where she worked on the assembly
line, slaughtering cattle and preparing them for packaging. She was exposed to
brain and spinal cord matter when she would euthanize the cattle. The husband
says that he does not know any fellow workers with a similar illness. He also
says that she did not have any preceeding illness or travel.

In 2009, a pathologist with sporadic Creutzfeldt–Jakob Disease (sCJD) was
reported to the Spanish registry. This case prompted a request for information
on health-related occupation in sCJD cases from countries participating in the
European Creutzfeldt Jakob Disease Surveillance network (EuroCJD). Responses
from registries in 21 countries revealed that of 8,321 registered cases, 65
physicians or dentists, two of whom were pathologists, and another 137
healthcare workers had been identified with sCJD. Five countries reported 15
physicians and 68 other health professionals among 2,968 controls or non-cases,
suggesting no relative excess of sCJD among healthcare professionals. A
literature review revealed: (i) 12 case or small case-series reports of 66
health professionals with sCJD, and (ii) five analytical studies on
health-related occupation and sCJD, where statistically significant findings
were solely observed for persons working at physicians' offices (odds ratio: 4.6
(95 CI: 1.2–17.6)). We conclude that a wide spectrum of medical specialities and
health professions are represented in sCJD cases and that the data analysed do
not support any overall increased occupational risk for health professionals.
Nevertheless, there may be a specific risk in some professions associated with
direct contact with high human-infectivity tissue.

A VERY IMPORTANT FACTOR that must
be weighed in on, HEALTH INSURANCE COMPANIES. IF there is not a provision,
clause, that stipulates that being placed AT RISK OF CREUTZFELDT JAKOB DISEASE,
would NOT blackball you i.e. MARK you, that NOT in any way can discriminate
against you because of the disease, that NOT in any way would jeopardize or
enhance cost for health insurance for anyone being placed 'AT RISK'.

I am deeply concerned about the answer given to
Lord Lucas on CJD andinsurance company's. In Her Majesty's reply, the reason
given forinsurance company's _not_ being able to require candidates for
lifeinsurance to be tested for incipient nvCJD or any human TSE, was because
there is no test to date, that would allow them to test.

My question to Her Majesty's Court would have
been;when such a test is available, will the insurance company's be
allowedto test for human TSE's?

It seems Lord Lucas question was not answered
fully, it seems HerMajesty's Court just went around the question.

If in fact, the insurance company's are allowed to
do this, once againthe people would have been deceived by their government,
for the sakeof money, greed, and corporate industry$$$ This would be
devastatingto the people, not only have they been murdered by corporate
greed,but they then would be sold out, for corporate greed. It's a
no-winsituation for public consumers...

kind regards,Terry S. Singeltary Sr., Bacliff,
Texas USA

April 4, 2000Lord Lucas asked Her
Majesty's Government:

Whether they will permit insurance companies to
require that candidates for life insurance be tested for
incipientnew-variant CJD.[HL1661]

Lord Hunt of Kings Heath: Insurance companies
would be unable tointroduce such a step, as no acceptable test currently
exists for the demonstration of infection before the onset of
clinicalsymptoms.

first Huntington's, then CJD, then another, and so
on.what needs to take place, is everyone drop their insurance.once you
give these people an opening, it's like a hole ina dam, there is no closing
it, and it just gets bigger and bigger. This is a serious breach of human
ethics, all for thealmighty dollar$$$

kind regards,Terry

DEPARTMENT OF HEALTH 2000/0580 Friday 13th October 2000 COMMITTEE ANNOUNCES DECISION ON USE OF GENETIC
TEST RESULTS FOR HUNTINGTON'S DISEASE BY INSURERS

The Genetics and Insurance Committee (GAIC) has
today announced that the reliability and relevance of the genetic test for
Huntington's Disease is sufficient for insurance companies to use the result
when assessing applications for life insurance.

Professor John Durant, Chairman of GAIC said:

"Genetic test results are already used in certain
circumstances by insurers and the Committee was asked to look at the
reliability and accuracy of the genetic test for Huntington's Disease. We
have considered carefully the application received from the Association
ofBritish Insurers for approval of the use of these tests. The evidence presented demonstrates that the two
tests for the Huntington's gene are reliable and that an abnormal result is
associated with significant clinical effects and with an increased
probability of a claim on a life insurance policy. This decision will
mean that those with a negative test result will not be asked topay more for
life insurance because of their family history of HuntingtonÆs disease. "This decision does not mean that individuals will
be asked to have agenetic test for Huntington's Disease before obtaining
insurance but,where individuals have already been tested as part of their
medical care, then there is nothing to prevent insurance companies asking
forthat information.

"Many who have a family history of a genetic
disorder such as Huntington's Disease have difficulty in obtaining insurance
because of their family history. The approval of the two tests for
Huntington's Disease will allow insurance to be provided at normal rates
to those who have a normal test result."

A significant amount of data has been collected
concerning the effects of Huntington's Disease on life expectancy and on
mortality risk as part of the process of reviewing this application. The
Committee hopes that the insurance industry will use this informationto
look at the problems of those who have an abnormal genetic test result and
of those who have chosen not to have a genetic test (who have a 50 % chance
of carrying the abnormal gene if they have an affected parent).

The GAIC was asked to examine the actuarial
evidence for using individual genetic tests. The insurance industry, through
the main trade body the Association of British Insurers, has agreed to abide
by GAIC decisions. If GAIC decides that the evidence on the reliability
and relevance of a particular test is insufficient to justify its use, the
Association have agreed to stop using them and retrospectively reassess
affected individual insurance premiums. Thebroader social and ethical issues
surrounding the use of genetic tests in insurance and employment have been
referred to the new HumanGenetics Commission.

An application for approval of two genetic tests
for Huntington's Disease was submitted to GAIC by the Association of British
Insurers (ABI) in July 2000. The application was sent to a clinical
geneticist and an independent actuary for expert review and also to
support groups for Huntington's Disease and to the Genetic Interest
Group (GIG) for their comments. At their meeting on 28 September, GAIC
considered the application, in the presence of observers from the ABI, GIG
and Huntington's Disease Association. Their decision isannounced today. The committee recognises that this complex subject
is an important issue to the public, industry and government alike. GAIC
will work closely with the new Human Genetics Commission when they begin
their inquiry into the use of genetic data including in insurance and
employment later this year.

Notes to Editors: A summary of the decision and further details
about GAIC and the application process are available on the Department of
Health web site at www.doh.gov.uk/genetics/gaic.htm

The establishment of the Genetics and Insurance
Committee (GAIC) on 12 April 1999 fulfilled the Government's commitment to
establish an independent review body, to evaluate the scientific and
actuarial evidence presented in support of the use of specific genetic tests
for insurance products. This was made in response to the Human Genetics
Advisory Commission (HGAC) report on the Implications of Genetic Testing for
the Insurance Industry, issued in December 1998. GAIC is a non-statutory Advisory Committee and has
a UK-wide remit. Its terms of reference are:

- to develop and publish criteria for the
evaluation of specific genetic tests, their application to particular
conditions and their reliability and relevance to particular types of
insurance; - to evaluate particular tests against those
criteria and promulgate its findings;

- to report to Health, Treasury and Department of
Trade and Industry Ministers on proposals received by GAIC from insurance
providers and the subsequent level of compliance by the industry with the
recommendations of GAIC.

The core membership of GAIC is: Professor John Durant, Chief Executive of
At-Bristol as Chairman, appointed from amongst the members of Advisory
Committee on Genetic Testing;

Professor Dian Donnai a geneticist nominated by
CMO (England); Dr David Muiry, an Actuary nominated by the
Faculty and Institute ofActuaries;

Mr Anthony OÆLeary, an Insurance Practitioner
nominated by the ABI; Mrs Susan Watkin and Mrs Barbara Carmichael,
members of Patient Support Organisations nominated by the Genetic Interest
Group; Professor Tim Bishop, an academic with a
background in epidemiology and genetics nominated by the Director of
Research, Department of Health.

GAIC has published evaluation criteria covering
the details of the genetic condition being tested for, the accuracy and
reliability of the tests used to detect it and the relevance of the test
results to decisions about insurance underwriting. GAIC expects that
applications will be for genetic conditions caused by changes in a
single gene, that are very likely to lead to serious ill health or
disability and that are therefore most relevant to the setting of
premiums for life and health insurance.

Over the next few months, GAIC will consider
applications relating tothe conditions currently covered by the Association
for British Insurers' Code of Practice on Genetic Testing. These include
Huntington's Disease, myotonic dystrophy, the early-onset form of
Alzheimer's disease and rare inherited cancers. The intention is to
complete review these applications by June 2001.

The Human Genetics Commission, chaired by Baroness
Helena Kennedy, was created in 1999 to provide the Government with strategic
advice on the wider implications of human genetics. It replaces three
formercommittees and is responsible for making links between all the other
relevant bodies in the advisory and regulatory framework. Further
information can be found at www.hgc.gov.uk

HGC has been formulating a public consultation
exercise on the storage, protection and use of personal genetic information
which will include the use of genetic data for insurance purposes. The
issues are due to be discussed at a public consultative meeting at the
Centre for Life, Newcastle-upon-Tyne in November 2000.

"Terry S. Singeltary Sr." wrote:> >
######### Bovine Spongiform Encephalopathy
#########> > Greetings List,>
> Talk about something that really stinks, this does. First> the
U.K. Government allows the Industry's involved to continue> to murder
(God only knows how many). Then they don't support them,> and to top it
off, they then allow the only hope one has to> get any kind of medical
care, they allow the insurers to bail> out on victims of this man-made
blunder. I thought Lord Lucas> asked this question to Her Majesty's
Court, and Her Majesty's> Court said;> > ######### Bovine
Spongiform Encephalopathy > #########>
> They replied that as there was no test they could not test, so
the> question did not arise!> > Ralph> > >
Did I miss something or have they not yet responded to this one?>
>> > Question 20: Whether they will permit insurance companies to
require > that> > customers be tested for incipient nvCJD.>
> Dear Lord Lucas,> > the question has arised again, and
should be confronted.> may i suggest that you ask this question again. it
would seem,> with a test so close to come about for the testing of
TSE's,> one would think, they are just preparing for the worse,
and> covering their butts, at the same time.> > Politics as
usual, but my God, have not these people suffered> enough, without the
Governments completely stripping them> from any help at all. Hell, you
should just take them out back> and shoot them........> >
kind regards,> Terry S. Singeltary Sr., Bacliff, Texas USA>
===========================================> > Thursday, 12
October, 2000, 11:28 GMT 12:28> UK Genetic test first for UK>
> Genetic tests can predict future illness> Insurers in the UK are
to be allowed to use> genetic test results to identify people
with> hereditary illnesses.> > The government will announce
on Friday that> insurers will be able to use those results to>
refuse cover or to push up premiums for those> born with genes that could
lead to fatal> conditions.> > The decision makes Britain
the first country to> approve the commercial use of gene>
technology in this way.> > The Genetics and> Insurance
Committee,> an advisory body> reporting to the> Department
of Health,> has decided that a test> used to identify a>
hereditary risk of> contracting the disease> Huntington's chorea
is> technically reliable.> > Tests covering several other
conditions,> including hereditary breast cancer and> Alzheimer's
disease, are also awaiting approval.> > Two years ago another
advisory body, the> Human Genetics Advisory Commission,>
recommended a moratorium on the use of> information from such
tests.> > However, that advice was rejected by the>
government, which decided insurers should be> able to use such
information, subject to the> Genetics and Insurance Committee agreeing
a> test's technical reliability.> > The announcement is
likely to fuel the ethical> debate over the use of genetic
information.> > Critics fear that vulnerable groups could find
it> difficult to get a mortgage or life insurance, or> face higher
premiums.> > But the insurance industry dismissed that>
suggestion.> > No compulsion> > Professor John
Durant, chairman of the> Genetics and Insurance Committee, told
the> BBC that nobody would be asked to take a> genetic test by an
insurance company.> > Rather they would be> expected to
disclose> the results of any> genetic test for>
Huntington's disease> they had taken in the> past.>
> Professor Durant said> this would not be a> legal
obligation, but> insurance companies> would have the right
to> refuse to offer> insurance if a customer> refused to
reveal details.> > He said: "It is not a punitive step. This
will> actually benefit very many people seeking>
insurance.> > "The only people who are likely to have
taken> a test for Huntington's disease are people with> a family
history of this disease.> > "Many of those people will actually
have had> results which show that they are fortunate> enough not
to have inherited the gene, so> those people will be able to get
insurance, at> the moment they may well find it difficult.">
> Mary Francis, the Director-General of the> Association of
British Insurers, said that> companies already asked potential
customers> about family history of disease.> > She said:
"This is really an extension of what> already does happen.">
> Sue Watkin, chair of> the Huntington's> Disease
Association,> also said insurance> companies were already>
using genetic test> results to calculate or> refuse
premiums.> > She said: "Our main concern is that people at>
risk of late onset genetic disorders should be> able to get insurance of
some kind up to a> certain level.> > "At present, many
people are made offers they> just cannot afford."> > Ms
Watkin said that a person at 50% risk of> developing Huntington's often
found their> insurance premium loaded by as much as> 300%.>
> She called on the government to establish a> fund to be used to
provide insurance for> people at risk.> > The National
Consumers' Council is concerned> people will be put off having tests
because> they feared that the results might count> against them -
with a possible knock-on effect> on their health.> > A
spokeswoman said: "A person might think if I> take a test I will know
information that I don't> know now, and maybe ignorance is bliss.>
> "If you don't know the information you can't> put it on the
form."> > The Human Genetics Commission, another>
government advisory body overseeing> developments in the use of
genetic> technology, said that it would launch shortly a> major
public consultation exercise about the> use and protection of genetic
information,> which would include insurance issues.> > The
exercise would eventually result in the> Commission making
recommendations to> ministers.> >
http://news.bbc.co.uk/hi/english/health/newsid_968000/968443.stm>

it just hit me about the blood testing. bought
knocked me out of thechair. could it be, the reason they have stalled the
blood testing, theyare waiting for the genetic testing to be perfected for
the insurancecompany's. once perfected and implemented, and no risk of any
typemedical insurance coverage for TSE patients, then they will be
allowedto go ahead with the blood tests for human TSE's. pretty smart huh,
theydon't pay all these Gov. Officials just to cram BSE tainted
hamburgersdown the throat of their daughters, or just for nothing. They pay
a goodportion of them to think up schemes, to get them out of
man-madeenvironmental death sentences. I would love to know, who
thoughtup the scheme, to brain-wash everyone into believing the 'CHOSEN
ONES'are the only ones tied to this man-made death sentence? Probably
thesame one to think up the genetic testing for insurance
companies.Oh, well, this pretty much does it for me today. Probably
alreadyover-loaded myself today. Now i know why Mr. Schmitt only allows
4messages.

"Terry S. Singeltary Sr." wrote:>>
######### Bovine Spongiform Encephalopathy
#########>> Greetings again list
members,>> Has anyone heard of any further development of the
Schmerr test???> I knew of powers within, that were trying to inhibit the
progress> of this testing (from a _most_ reliable source), but did not
think they> actually would stop the research.>> hmmmm, who
knows???>> Here are a few links some may find
informative;>> Opinion On> Update of the Opinion given by
the Scientific Committee on Medicinal> Products and Medical Devices on
The Risk Quantification For CJD> Transmission Via Substances of Human
Origin;>> 2. Screening assays>> It is assumed that
although there is no proven or even probable case of> transmission by
blood or blood products the identification and exclusion> of donors in
the preclinical phase of CJD or vCJD would contribute to an> increase in
the safety margin and, probably, an increase in the> confidence in blood
and blood products by potential recipients.> Therefore, the SCMPMD in its
Opinion of October 1998 emphasised the need> for "the development of a
simple readily available ex vivo diagnostic> test for preclinical
nvCJD/CJD". In addition it stated: "When a> validated test for TSE
infectivity in donor blood becomes available, it> should be implemented
in routine donor screening as soon as possible and> donors found to be
positive should be excluded from donation. Member> Statos should, in the
interest of public health, warrant availability of> TSE tests for blood
screening in collaboration with possible patent>
holders.">> During the "WHO Consultation on Diagnostic Procedures
for Transmissible> Spongiform Encephalopathies: Need for Reference
Reagents and Reference> Panels" held in Geneva on March 22 and 23, 1999,
M.J. Schmerr presented> results of a new assay that may be able to detect
the pathological fbrm> of ption protein in blood of animals in the
clinical as well as in the> preclinical phase of TSE (serapie in sheep
and chronic wasting disease> in deer, Schmerr 1999, Schmerr et al. 1999).
The basic reaction is the> competition of the proteinase K treated sample
with a labelled peptide> derived from the sequence of prion protein
binding to an antibody mised> against this peptide (Schmerr et al. 1998).
The test material is> extracted from buff), coat prepreed from a sample
of peripheral blood.> >From the relation between ti'ee and bound
peptide as determined by> capillary electropheresis the amount of
corn?ting protein i.e. protease> resistant prion protein, is
calculated.>> In contrast to other tests used for the detection of
TSE infected> animals or lbr confirmation of CJD/vCJD in humans the assay
proposed by> Schmerr uses for the first time as test material a body
fluid, namely> blood, which is eaqily availahl,~ In thi~ respect, this
assay fulfils a> prerequisite for a screening assay which could be used
in the blood> donation setting. However, it has to be stressed that this
assay is far> from ir~ing vaildated tidier in animals or in humans. On
the contrary,> preliminary tests with haman material performed in several
laboratories> have not yet validated this test.>> There is
no doubt that the assay has the potential to be developed into> a
screening assay, but this developmere will need a number of carefully>
designed studies. Use in donor screening will not be possible until>
there is more information on the sensitivity, specificity and validity>
of the assay.>> The SCMPMD repeats its recommendation to support
efforts in the> development of easily applicable screening tests for
CJD/vCJD.>> The SCMPMD would also like to draw the attention to an
ethical aspect of> the expected introduction of a screening assay for
CJD/vCJD. The> information of a positive test result would confront the
individual with> the diagnosis of an inevitably fatal disease without any
reliable> prediction of the duration of the preclinical phase. Such
information> could cause severe psychological stress and would demand
careful> counselling. In such a situation, it would not be surprising if
donors> would stop donating il' such a test for CJD/vCJD were introduced.
If the> number of those dollors is high the introduction of a screening
assay> would lead to a significant loss of donors who would have to be
replaced> by first time donors who are at higher risk of well known blood
borne> infections. This situation should be considered well in
advance.>> 3. Exclusion of donors at risk for TSE infection by
ruminant derived> material>> Until the end of 1998 vCJD
cases were observed only in the United> Kingdom (UK), with one single
exception. Therefore, residency in UK was> described as one of the known
risk factors for vCJD (the others being> young age (i.e. below 53 years)
and homozygosity of methionine at codon> 129 of the prion protein gene).
The exclusion of donors who resided for> some time in the UK could,
therefore, be considered as contributing to> minimising the theoretical
risk of vCJD transmission by blood and blood> products.>>
The first recommendation of this kind was given by the Ottawa based>
Bayer Advisory Council on Bioethics which stated in his working paper>
"Creutzfeldt-Jakob disease, blood and blood products: A bioethics>
framework" (1998):> "The differences between classical CJD on the one
hand and nvCJD on the> other creme differences in the quality of the
hypothetical risk. As> discussed earlier, the new variant form appears to
have crossed the> species barrier from cattle. It has an earlier age at
onset, and the los> of pathological ptiohs is much greater than in
classical forms of the> disease. The anatomical distribution of nvCJD
infectivity is also> different, which raises the plausible possibility
that it is more likely> to have infectivity in the blood. Therefore,
nvCJD is the wild card that> warrants special vigilance. The disease
appears to be isolated, at> present, to parts of Europe. The number of
people in affected countries> who are currently incubating the disease is
ankhown. The Council> therefore recommends:>> 20. That
persons who, at any time since 1980, have resided in a> geographic area
with a significant incidence of BSE or nvCJD not be> permitted to
contraute blood or plasma until the hypothetical risk of> accepting
donations from such persons can be evaluated.">>
http://europa.eu.int/comm/food/fs/sc/scmp/out28_en.pdf>> also, for
those interested, here are more documents on this and> other
issues;>>
http://europa.eu.int/comm/food/fs/sc/scmp/out12_en.pdf>
http://europa.eu.int/comm/food/fs/sc/scmp/out20_en.html>
http://europa.eu.int/comm/food/fs/sc/scmp/out25_en.html>
http://europa.eu.int/comm/food/fs/sc/scmp/out29_en.pdf>> kind
regards,> Terry S. Singeltary Sr., Bacliff, Texas USA

2011

According to advisers to the British government, though the test is
undoubtedly a significant step towards eliminating the incurable disease and
preventing it from becoming endemic in society, it could result in a reduction
in the number of blood donors and there are also fears it could increase
insurance premiums.

Experts suspect that donors will be
reluctant to give blood if they risk being told that they have the possibility
of developing the disease which causes a horrible and agonising
death.

Dr. John Forsythe, chair of the Advisory Committee on the Safety of
Blood Tissues and Organs (SABTO) and a transplant surgeon at the Royal Infirmary
of Edinburgh says the test does have significant downsides, despite concerns
that the disease could become widespread in the UK.